主动脉弓狭窄心衰模型 z-bo 2020-12-09 331

　　Objective To establish a stable and reliable mouse heart failure model by non-thoracic aortic arch stenosis, and to analyze and observe the pathological process of heart failure in mice.

　　Methods The C57BL/6J mouse heart failure model was established by non-thoracotomy TAC, and the cardiac function and the degree of heart failure were evaluated by echocardiographic imaging, left ventricular mass index, and histopathological examination. Results The left ventricular mass index gradually increased over time. Compared with the sham operation group, there were very significant differences at 4, 8 and 12 weeks after the operation (P<0.01). The echocardiography showed that it was similar to the sham operation group. Compared with the four weeks after TAC, the left ventricular anterior wall thickness, left ventricular corrected weight (LVmasscorreted), heart rate (HR), and cardiac output (Cardiacoutput, CO) increased significantly (P<0.01), 8 weeks after surgery Left ventricular wall thickness, left ventricular corrected weight and left ventricular end-systolic volume (LV Vols) increased significantly (P<0.01), ejection fraction (ejection fraction, EF) and short axis rate (fractional shortening (FS) significantly decreased P<0.01), 12 weeks after TAC, left ventricular end diastolic diameter (LVID, d), left ventricular end systolic diameter (LVID, s), left ventricular end diastolic volume (LVVol, d) and left ventricular end systole The volume (LVVol, s) increased significantly (P<0.01), and the ejection fraction and short axis rate were further reduced (P<0.01). At the same time, pathological examination showed that myocardial fibers were abnormal or diseased in varying degrees.

　　 Conclusion The experimental results show that the establishment of a mouse heart failure model using non-thoracic TAC is stable and feasible, and can simulate the pathophysiological process from left ventricular hypertrophy to heart failure caused by human pressure overload.